Atrial fibrillation is the most common cardiac arrhythmia. It creates rapid quivering of the upper chambers of the heart. Acute symptoms can include palpitations, chest pain, shortness of breath and dizziness. Prolonged arrhythmia can result in significant morbidity by potentially causing congestive heart failure and/or stroke.
Theoretical and computational cardiac models have helped to confirm that during arrhythmia the electrical wavefront transmitted through the heart causing contraction or a heartbeat degenerates into one or more rotors. Rotors exhibit a characteristic spiral-shaped wave front of depolarization from a core of affected cells. A rotor's spiral waves present as a repetitive cycle of electrical activation around the central core.
The current understanding of atrial fibrillation in humans requires a coordination of two main events. First, an initiating cardiac electrical impulse or trigger occurs elsewhere than the normal sinus node pacemaker of the heart. This trigger most commonly originates from sleeves of cardiac tissue at the opening of the pulmonary veins within the left atrium but may also emanate from non-pulmonary vein sites or even degenerate from reentrant circuits (sites from which the cause of the arrhythmia is due to the electric signal not moving in a single wave front from the atria to the ventricles as in the normal circuit, but rather as a circuit looping back upon itself). The second event is rotor formation. A rotor develops when the depolarizing electrical impulse that propagates away from a trigger in the form of a wave front undergoes a wave break, turning on an axis. The turning wave front is believed to be a result of regional changes in structure, fibrosis, fiber orientation, autonomic innervation, local conduction velocity characteristics, and/or refractory periods. The curved wave front of the rotor can create a self-sustaining circular trajectory that spins around its rotor core, called a phase singularity. A rotor can spin fairly fast, with any one rotor having a characteristic cycle length. Cycle lengths have been documented in ranges of about 130 to about 210 milliseconds and are stable over time, for instance up to tens of minutes. It has been postulated that atrial fibrillation is maintained by a small number (1-2) of high frequency rotors that drive the continuation of the atrial fibrillation. In the case of multiple simultaneous rotors, the rotor exhibiting the highest frequency is considered the driving rotor. High frequency rotors occur more frequently in the left atrium, resulting in a gradient of atrial fibrillation drivers from left to right chambers.
Treating atrial fibrillation by ablation of trigger sites and rotors has shown better results in maintaining sinus rhythm and quality of life as compared to medical therapy. Much investigation is ongoing to further improve acute success rates and longevity of being arrhythmia-free, with mapping and ablation of rotor sites being added to accepted methods of atrial fibrillation ablation.
There are currently two commercially available methods for mapping of rotors. Dominant frequency mapping involves time consuming point-by-point recording of the electrical activity within the heart. Each recording is analyzed by spectral analysis to determine each specific site's most stable dominant frequency. A site-specific recording may provide information about that point, but does not provide much information about whether a rotor is nearby. Trying to find a rotor or the path along which a rotor precesses is by hunt-and peck without any guidance as to where to try next.
The second method uses a basket catheter to record electrical activity simultaneously from 64 electrodes (8 electrodes over each of 8 splines). The simultaneous local electrical activity of the atrial chamber is displayed panoramically in 2 dimensions. Recording by basket catheters also presents challenges. Stable electrode contact can be problematic but is required to record, compute and display cardiac electrical activity. Unfortunately, many patients with persistent forms of atrial fibrillation have enlarged atria that can be significantly larger than the basket itself. This results in the substantial technical limitation of not having adequate tissue contact for many of the electrodes. In addition, electrode spacing ranges between 4 to 8 mm along splines, depending on basket size, and full expansion of the largest basket catheter to a diameter of 6 cm results in electrode separation between splines of about 2.5 centimeters. Rotor diameters are estimated to be about 1.5 cm to 2 cm. Thus, the basket geometry allows for only one or two at most electrodes on the catheter to record within a rotor site. The consequential wider spline separation of basket catheters in these enlarged atria diminishes the probability to accurately identify a rotor location.
What are needed in the art are devices and methods for mapping cardiac tissue and thereby recognizing locations of interest during cardiac arrhythmia. For instance, improved ability to map, identify and ablate rotors would be of great benefit. Presently, a rotor site cannot be identified by standard recording techniques and requires color activation time maps. A device and method that can provide for immediate rotor detector/locator, an ectopic site detector/locator and a circuit locator would be of great benefit.